Genetic Signature for Type 2 Diabetes Risk May Have Been Identified
Scientists believe they've finally pinpointed the genetic reason some people get Type 2 diabetes while others with similar lifestyles do not. The Type 2 diabetes signature has been known for some time, but not very well understood. A new study has determined that some of those signature links may change the way certain cells in the pancreas operate.
The genes specifically affect how certain pancreatic cells "read" their genetic code. These DNA-reading molecules are part of Regulatory Factor X (RFX), which is a "master regulator" for a number of genes.
The findings could lead to personalized treatments for Type 2 diabetes.
A new paper in the Proceedings of the National Academy of Sciences outlines the findings. Those findings are the property of cooperative research between the University of Michigan, the National Institutes of Health, the Jackson Laboratory for Genomic Medicine, the University of North Carolina, and the University of Southern California.
Many diabetes-linked DNA changes affect the ability of RFX to bind to specific locations in genomes of pancreas cell clusters (called islets). This in turn affects the cells' ability to function.
"We have found that many of the subtle DNA spelling differences that increase risk of Type 2 diabetes appear to disrupt a common regulatory grammar in islet cells," says Stephen C.J. Parker, Ph.D., an assistant professor of computational medicine and bioinformatics, and of human genetics, at the U-M Medical School. "RFX is probably unable to read the misspelled words, and this disruption of regulatory grammar plays a significant role in the genetic risk of Type 2 diabetes."
The researchers note that this same process could be part of a neonatal diabetes that is particularly fatal.
Source: ns.UMich.edu
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